|Table of Contents|

Dihydrokaempferol derivatives inhibit palmitic acid-induced lipid deposition in C2C12 myotubes through AMPK/PGC-1α pathway

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《第三军医大学学报》[ISSN:1000-5404/CN:51-1095/R]

Issue:
2017年第16期
Page:
1606-1611
Research Field:
基础医学
Publishing date:

Info

Title:

Dihydrokaempferol derivatives inhibit palmitic acid-induced lipid deposition in C2C12 myotubes through AMPK/PGC-1α pathway

Author(s):

GU Yeyun ZHOU Qicheng GONG Xinhua ZHU Jundong MI Mantian

Department of Nutrition and Food Hygiene, Chongqing Key Laboratory of Nutrition and Food Safety, Chongqing Center of Medical Nutrition, College of Military Preventive Medicine, Third Military Medical University, Chongqing, 400038, China

Keywords:

dihydrokaempferol skeletal muscle: lipid deposition AMP-activated protein kinase peroxisome proliferator activator receptor gamma coactivator-1alpha

PACS:
R151.3; R329.26; R587
DOI:
-
Abstract:

Objective     To determine the effects of 4 derivatives from dihydrokaempferol on lipid deposition in C2C12 myotubes (C2C12-MD cells) and investigate the underlying mechanisms. Methods      Mouse C2C12 myoblasts were differentiated into myotubes and then treated by palmitic acid (PA) alone or in combination with 4 derivatives of dihydrokaempferol (kaempferol, dihydromyricetin, myricetin and quercetin) respectively. Lipid deposition was evaluated by oil red O staining and triglyceride (TG) content measurement. Glucose uptake was measured by using 2-NBDG fluorescent probe. The protein levels of AMP-activated protein kinase (AMPK), phosphorylated AMPK (p-AMPK) and peroxisome proliferator activator receptor gamma coactivator-1alpha (PGC-1α) were detected by Western blotting. Results    PA induced more lipid deposition, significantly increased TG content, and significantly decreased glucose uptake under insulin stimulation as well as the protein levels of pAMPK and PGC-1α in C2C12 myotubes (P<0.05). Kaempferol treatment had no significant effects on these changes induced by PA. However, the other 3 derivatives markedly inhibited these changes induced by PA, and dihydromyricetin showed a stronger inhibitory effect (P<0.05). Moreover, AMPK inhibitor compound C could significantly reverse the inhibitory effect of dihydromyricetin (P<0.05). Conclusion      Three derivatives of dihydrokaempferol (dihydromyricetin, myricetin and quercetin) inhibit PA-induced lipid deposition in C2C12-MD cells through AMPK/PGC-1α signaling pathway, and thereby improve insulin resistance.

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Last Update: 2017-08-18